中文摘要：

背景在 acetabular 发育异常的病理学的变化的顺序和机制仍然是不清楚的。调查软骨在 27 只 1-month-old 新西兰兔子经历了的不同 ages.Methods 在兔子 acetabular 发育异常模型改变的这研究在膝扩展扔了左后部的手足的固定。连续 acetabular 发育异常模型被对 acetabular 索引并且突然地的评价建立的拍上的角度。acetabular 软骨的厚度在一台显微镜下面被测量，并且纤维变性被观察。Ultrastructural 变化与扫描电子显微镜学和传播电子显微镜学被调查。骨胶原的送信人 RNA 表示并且， 1 integrin，和 caspase-9 被即时荧光测量在兔子的一个不成熟的组的量的聚合酶链 reaction.Results，对待的臀部的 acetabular 索引与动物生长增加了。左髋臼的边缘上的软骨在右边上是比那显著地厚的。软骨的表面上的骨胶原纤丝变得粗野，并且在增大层的 chondrocytes 经历了坏死。在兔子的一个成熟的组，左突然地是与 6 星期的扔在兔子增加的角度。左髋臼的边缘上的软骨经历了纤维变性。chondrocytes 微弱地被染色，并且 lysosomes 的数字比正常大得多。骨胶原的送信人 RNA 表示并且，在软骨的 1 integrin，和 caspase-9 在增加纤维变性跟随的厚度的不同 ages.Conclusions 显著地不同可以是在 acetabular 发育异常的病理学的软骨变化的顺序，与在贡献这个过程的超微结构和骨胶原表示的变化。

英文摘要：

Background The order and mechanism of pathological changes in acetabular dysplasia are still unclear. This study investigated cartilage changes in rabbit acetabular dysplasia models at different ages.Methods Twenty-seven 1-month-old New Zealand rabbits underwent cast immobilization of the left hind limb in knee extension. Serial acetabular dysplasia models were established by assessment of the acetabular index and Sharp＇s angle on radiographs. The thickness of the acetabular cartilage was measured under a microscope, and fibrosis was observed. Ultrastructural changes were investigated with scanning electron microscopy and transmission electron microscopy. The messenger RNA expression of collagen Ⅰ and Ⅱ, β1 integrin, and caspase-9 were measured by real-time fluorescence quantitative polymerase chain reaction.Results In an immature group of rabbits, the acetabular index of the treated hip increased with animal growth. The cartilage on the brim of the left acetabulum was significantly thicker than that on the right side. The collagen fibrils on the surface of the cartilage became gross, and the chondrocytes in the enlargement layer underwent necrosis. In a mature group of rabbits, the left Sharp＇s angle increased in the rabbits with 6-week casting. The cartilage on the brim of the left acetabulum underwent fibrosis. The chondrocytes were weakly stained, and the number of lysosomes was much larger than normal. The messenger RNA expression of collagen Ⅰ and Ⅱ, β1 integrin, and caspase-9 in the cartilage differed significantly at different ages.Conclusions Increasing thickness followed by fibrosis may be the order of pathological cartilage changes in acetabular dysplasia, with changes in ultrastructure and collagen expression contributing to the process.